Fig. 44.23A , Late Follicular Phase).
Event 6: Once the dominant follicle causes circulating estrogen levels to exceed 200 pg/mL for about 50 hours in women, estrogen exerts a positive feedback on the gonadotrope to produce the midcycle LH surge. This is enhanced by the small amount of progesterone secreted at midcycle. The exact mechanism of the positive feedback is unknown, but it occurs largely at the level of the pituitary. GnRH receptors and the sensitivity to GnRH signaling increase dramatically in the gonadotropes. The hypothalamus contributes to the gonadotropin surge by increasing the frequency of GnRH pulses.
Event 7: The LH surge drives meiotic maturation, ovulation, and differentiation of granulosa cells into progesterone-producing cells (see
Fig. 44.23A , Late Follicular Phase).
Event 8: Rising levels of progesterone, estrogen, and inhibin A by the mature corpus luteum negatively feed back on pituitary gonadotropes. Even though estradiol levels exceed the 200-pg/mL threshold for positive feedback, the high progesterone levels now produced by the corpus luteum block any positive feedback of estradiol. Consequently both FSH and LH levels decline to basal levels (see
Fig. 44.23B , Mid-Luteal Phase).
Event 9: Basal levels of LH (but not FSH) are absolutely required for normal corpus luteum function. However, the corpus luteum becomes progressively insensitive to LH signaling and will die unless LH-like activity (i.e., hCG from an implanted embryo) increases. In a nonfertile cycle the corpus luteum of menstruation will regress in 14 days, and progesterone and estrogen levels will start to decline by about 10 days, thereby cycling back to event 1 (see
Fig. 44.23B , Late Luteal Phase).